We investigated the relative contribution of humoral (carbon dioxide) and neural (trigeminal stimulation) inputs in the cerebrovasodilatory response to simulated diving in the rat. The cerebral hemodynamic profile of rats was determined using the brain blood flow tracer N-[¹⁴C]isopropyl-p-iodoamphetamine. During a simulated dive response, cerebral vascular resistance (CVR) decreased 63.1%, resulting in a 1.5-fold increase in cerebral blood flow (CBF). To investigate the contribution of hypercapnia to the decrease in CVR during simulated diving, we measured CBF during simulated diving in rats with preexisting hypocapnia. To investigate the contribution of trigeminal input, we measured CBF during periods of trigeminal stimulation alone with continued ventilation. Preexisting hypocapnia abolished the cerebrovasodilatory response to simulated diving. Trigeminal stimulation alone did not produce a significant increase in CBF from control values in any brain region, suggesting that trigeminal input does not contribute to the cerebrovascular response to simulated diving in rats. These results suggest that the cerebrovasodilatory response observed during diving in small mammals is driven primarily by progressive hypercapnia associated with asphyxia.